Based on the predicted crystal structure of CYP8A1( *)5 using the Molecular Operating Environment platform, the distance from CYP8A1 Cys441 to the heme was altered with a significantly changed binding free energy for the mutant protein.

results indicate that PGIS expression was associated with radiotherapy efficiency

In a case-control study unaffected carriers of a BMPR2 mutation, linked to pulmonary artery hypertension (PAH), were most often found to have prostacyclin synthase promoter sequence variants, which were thought to protect against PAH.

These findings suggest that PGIS is induced by hypoxia and regulates the expression of VEGF in fibroblasts.

High PTGIS expression is associated with colorectal cancer hepatic metastasis.

Sepiapterin not only reversed the effects of high glucose on both angiotensin II-induced relaxation and PGI(2 (show PTGIR ELISA Kits)) release but also abolished high-glucose-enhanced PGIS nitration.

Alpha(2)-adrenoreceptor activation is required for coupling heart rate to central inspiratory drive during acute hypoxia, and PGI(2 (show PTGIR ELISA Kits)) is required to enhance the inhibition of sympathoactivation.

The results provide strong evidence that the protective effects of COX-2 (show COX2 ELISA Kits) within the liver are mediated through the production of PGE (show LIPF ELISA Kits)(2) and PGI(2 (show PTGIR ELISA Kits)), which exert anti-inflammatory functions.

Prostaglandin I2 (Prostacyclin) Synthase (PTGIS) Antigen Profile

Antigen Summary

This gene encodes a member of the cytochrome P450 superfamily of enzymes. The cytochrome P450 proteins are monooxygenases which catalyze many reactions involved in drug metabolism and synthesis of cholesterol, steroids and other lipids. However, this protein is considered a member of the cytochrome P450 superfamily on the basis of sequence similarity rather than functional similarity. This endoplasmic reticulum membrane protein catalyzes the conversion of prostglandin H2 to prostacyclin (prostaglandin I2), a potent vasodilator and inhibitor of platelet aggregation. An imbalance of prostacyclin and its physiological antagonist thromboxane A2 contribute to the development of myocardial infarction, stroke, and atherosclerosis.